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17 Cards in this Set

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Regulation and maintenance of arterial blood pressure--why is it so important?
• There's a need for consistently high pressure in the main arteries (elastic or conducting arteries)--brachial, femoral, etc. Pressure ensures volume and flow for the tissues.

• Local control occurs at the organ/tissue level by arterioles.
Identify what each line represents:
Identify what each line represents:
Note right atrial pressure--fairly low, but during diastole it approximates LV pressure. (LVEDP)
Discuss neural mechanisms for regulating BP:

Discuss hormonal mechanisms for regulating BP:
Neural:
•  Autonomic nervous system
•  Fast acting, but short-term effects
•  Heart rate, contractility, total peripheral resistance

Hormonal:
•  Renin-Angiotensin-Aldosterone system
•  Slow acting, but long-term effects
•  Bl...
Neural:
• Autonomic nervous system
• Fast acting, but short-term effects
• Heart rate, contractility, total peripheral resistance
-Baroreceptors are key to this. They kick in in just seconds, but only have so much effect.

Hormonal:
• Renin-Angiotensin-Aldosterone system is key.
• Slow acting, but long-term effects
• Blood volume
-Slow to act (~a day), but has great effect (infinite on graph).
Discuss the Frank-Starling relationship:

What three things are tightly correlated in this relationship?
Cardiac output must equal venous return.
•  Increased VEDV causes increased stroke volume.

Maintained by the length-tension relationship of cardiac muscle.
•  Increased pre-load causes increased stroke volume.

Strong correlation betwee...
Cardiac output MUST EQUAL venous return.
• Increased VEDV causes increased stroke volume.

Maintained by the length-tension relationship of cardiac muscle.
• Increased pre-load (thus increased VEDV) causes increased stroke volume.

There's a strong correlation between VEDV, right atrial pressure, and venous return.
Discuss cardiac and vascular function curves:
We can graph both cardiac output and venous return as a function of right atrial pressure, and see how the two interact to determine the steady-state operating point.

*Cardiac function curve is basically the Frank-Starling curve.

*Venous ret...
*We can graph both cardiac output and venous return as a function of right atrial pressure, and see how the two interact to determine the steady-state operating point.

*Cardiac function curve is basically the Frank-Starling curve.

*Venous return (vascular function curve) has an inverse relationship to right atrial pressure:
-Pressure differences drive flow.
-The "knee" is the left, flat part of venous return line. Venous return flattens out because veins will collapse if there's a negative pressure on a vein.
-Note Mean systemic pressure.

*Curves intersect at the steady-state operating point; where Cardiac output = venous return
Discuss positive and negative inotropic effects:
Same VEDV (= same preload), but change in contractility. Changes the slope of the cardiac function curve.

Increased contractility due to:
•  Sympathetic stimulation
•  Sympathomimetic drugs (digitalis)
•  Antimuscarinic drugs

Decrea...
Same VEDV (= same preload), but change in contractility. Changes the slope of the cardiac function curve.

Increased contractility (increased EF, decreased RA pressure) due to:
• Sympathetic stimulation
• Sympathomimetic drugs (digitalis)
• Antimuscarinic drugs (anti-parasympathetic)

Decreased contractility (decreased EF, increased RA pressure) due to:
• Parasympathetic stimulation
• Parasympathomimetic or sympatholytic drugs (beta blockers)
Discuss changes in blood volume:

How do they change the cardiac and vascular function curves?

How do you change the blood volume?
*Changes the intercept of the vascular function curve.

Two ways to do this:
•  Change total volume.
•  Re-distribute volume; move blood between stressed and unstressed volumes.

A= unstressed to stressed shift; increased venous tone = d...
*Changes the intercept of the VASCULAR function curve.
-Increased blood volume increases RA pressure, mean systemic pressure, and CO.
-Decreased blood volume decreases RA pressure, mean systemic pressure, and CO.

Two ways to do this:
• Change total volume.
• Re-distribute volume; move blood between stressed and unstressed volumes.

A= unstressed to stressed shift; increased venous tone = decreased venous compliance.

B= stressed to unstressed shift; decreased venous tone = increased venous compliance.
Discuss circulatory shock in general--it's characterized by what 3 things?

Discuss the 5 types of it.
Circulatory shock- decreased blood flow, perfusion, O2 delivery.

1) Hypovolemic -whole blood (hemorrhagic shock), plasma volume (burn), fluid and electrolytes (vomiting, diarrhea)
2) Cardiogenic - myocardial impairment (infarction, CHF) 
3) M...
-Big ∆ in Blood Volume!
Circulatory shock- decreased blood flow, perfusion, O2 delivery.

1) Hypovolemic -whole blood (hemorrhagic shock), plasma volume (burn), fluid and electrolytes (vomiting, diarrhea)
2) Cardiogenic - myocardial impairment (infarction, CHF)
3) Mechanical obstruction - localized decreased flow. Cardiac tamponade or pneumothorax.
4) Neurogenic - loss of vasomotor tone (damage to brainstem sympathetic function or something like that)
5) Septic or anaphylactic - increased filtration across capillary walls
Discuss changes in Total Peripheral Resistance:

How do they change the cardiac and vascular function curves?
*Arteriole smooth muscle (changing vasomotor tone), changes afterload.

*Effects both curves.
*Arteriole smooth muscle (changing vasomotor tone), changes afterload.

*Everything shifts DOWN.

*Effects both curves.
Discuss neural control by the baroreceptor reflex:
*Parasympathetic and Sympathetic effects 
*Afferents in IX & X
*Parasympathetic and Sympathetic effects
*Afferents of the reflex are in IX (Hering's nerve) & X (vagus: aortic baroreceptors)

*Aortic arch, carotid body, carotid sinus contain baroreceptors.

*The more stretched out they are, the greater the firing rate.
Activity in the Carotid Sinus Nerve:
An example of baroreceptor action showing APs in a single axon related to blood pressure.
Schematic of baroreceptor feedback to brainstem and control of heart and blood vessels:

Where in the heart is control effected?
Which part of the ANS affects contractility?
Where is the greatest effect on blood vessels?
How does the nervous system alter TPR?
Responsiveness of the baroreceptor reflex:
Most responsive to changes in the normal operating range, and most responsive to rapid changes, system does adapt.
Most responsive to changes in the normal operating range, and most responsive to rapid changes.

System does adapt, so in the long term baroreceptors aren't useful.
Effectiveness of the baroreceptor reflex:
Most responsive to changes in the normal operating range, and most responsive to rapid changes, system does adapt.
Very effective! On the bottom, Hering's nerve has been cut.
Other neural mechanisms:

How do we get blood to the brain?
Chemoreceptors:
O2 receptors in carotid body and aortic arch. Mainly control breathing in response to low O2 (high CO2 and low pH potentiate). Arterial vasoconstriction in skeletal muscle, renal, and splanchnic vasculature. Blood flow is redirect...
*Chemoreceptors:
O2 receptors in carotid body and aortic arch. Mainly control breathing in response to low O2 (high CO2 and low pH potentiate). Arterial vasoconstriction in skeletal muscle, renal, and splanchnic vasculature. Blood flow is redirected to the lungs and brain!

*CNS ischemic response:
Chemoreceptors in the medulla, sensitive to increased CO2 and decreased pH. Increase sympathetic outflow from the vasoconstrictor center. Intense vasoconstriction in many non-brain vascular beds. Re-direction of blood flow and pressure to the brain!
Hormonal control of BP:
*Afferents in the JGA of the kidney.
pro-renin --> renin, etc.

*Ultimate effect is to increase blood volume and pressure.

*Long term control. Takes time to kick in.
Formula for BP:
BP = CO x TPR

= heart pushing x vessels pushing back